TY - JOUR
T1 - The physiology and pathophysiology of nitric oxide in the brain
AU - Guix, FX
AU - Uribesalgo, I
AU - Coma, M
AU - Munoz, FJ
PY - 2005/6
Y1 - 2005/6
N2 - Nitric oxide (NO) is a molecule with pleiotropic effects in different tissues. NO is synthesized by NO synthases (NOS), a family with four major types: endothelial, neuronal, inducible and mitochondrial. They can be found in almost all the tissues and they can even co-exist in the same tissue. NO is a well-known vasorelaxant agent, but it works as a neurotransmitter when produced by neurons and is also involved in defense functions when it is produced by immune and glial cells. NO is thermodynamically unstable and tends to react with other molecules, resulting in the oxidation, nitrosylation or nitration of proteins, with the concomitant effects on many cellular mechanisms. NO intracellular signaling involves the activation of guanylate cyclase but it also interacts with MAPKs, apoptosis-related proteins, and mitochondrial respiratory chain or anti-proliferative molecules. It also plays a role in post-translational modification of proteins and protein degradation by the proteasome. However, under pathophysiological conditions NO has damaging effects. In disorders involving oxidative stress, such as Alzheimer's disease, stroke and Parkinson's disease, NO increases cell damage through the formation of highly reactive peroxynitrite. The paradox of beneficial and damaging effects of NO will be discussed in this review. (c) 2005 Elsevier Ltd. All rights reserved.
AB - Nitric oxide (NO) is a molecule with pleiotropic effects in different tissues. NO is synthesized by NO synthases (NOS), a family with four major types: endothelial, neuronal, inducible and mitochondrial. They can be found in almost all the tissues and they can even co-exist in the same tissue. NO is a well-known vasorelaxant agent, but it works as a neurotransmitter when produced by neurons and is also involved in defense functions when it is produced by immune and glial cells. NO is thermodynamically unstable and tends to react with other molecules, resulting in the oxidation, nitrosylation or nitration of proteins, with the concomitant effects on many cellular mechanisms. NO intracellular signaling involves the activation of guanylate cyclase but it also interacts with MAPKs, apoptosis-related proteins, and mitochondrial respiratory chain or anti-proliferative molecules. It also plays a role in post-translational modification of proteins and protein degradation by the proteasome. However, under pathophysiological conditions NO has damaging effects. In disorders involving oxidative stress, such as Alzheimer's disease, stroke and Parkinson's disease, NO increases cell damage through the formation of highly reactive peroxynitrite. The paradox of beneficial and damaging effects of NO will be discussed in this review. (c) 2005 Elsevier Ltd. All rights reserved.
KW - Amyotrophic-lateral-sclerosis
KW - Vascular smooth-muscle
KW - Dependent protein-kinase
KW - Synthase messenger-rna
KW - Transgenic mouse model
KW - Nerve growth-factor
KW - Nf-kappa-b
KW - Programmed cell-death
KW - Amyloid beta-peptide
KW - Experimental autoimmune encephalomyelitis
KW - Nitric oxide
KW - Brain
UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-24144494527&origin=inward
UR - https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=pure_univeritat_ramon_llull&SrcAuth=WosAPI&KeyUT=WOS:000232313300003&DestLinkType=FullRecord&DestApp=WOS
U2 - 10.1016/j.pneurobio.2005.06.001
DO - 10.1016/j.pneurobio.2005.06.001
M3 - Review
C2 - 16115721
SN - 0301-0082
VL - 76
SP - 126
EP - 152
JO - Progress in Neurobiology
JF - Progress in Neurobiology
IS - 2
ER -